Randomized controlled trial of duration of analgesia following intravenous or rectal acetaminophen after adenotonsillectomy in children.

BACKGROUND: Doses of acetaminophen 40 mg kg(-1) rectally and 15 mg kg(-1) i.v. produce similar effect-site concentrations. However, the clinical effectiveness of these routes has not been compared. The aim of this study was to compare duration and efficacy of analgesia in children following adenotonsillectomy after acetaminophen either 40 mg kg(-1) rectally or 15 mg kg(-1) i.v. METHODS: Fifty children aged between 2 and 5 yr were recruited. They received a standardized anaesthetic, including 2 microg kg(-1) of fentanyl. Children were randomized to receive either rectal or i.v. acetaminophen. Postoperative pain was assessed regularly with the Children and Infants Postoperative Pain Scale score and rescue analgesia provided if scores were 4 or greater. The primary outcome measure was time to first analgesia. Results were plotted with a Kaplan-Meier analysis and median time to rescue analgesia compared between the groups. RESULTS: The protocol was successfully completed in 46 children. Forty-five children required rescue medication. The time to first rescue analgesia was longer in children receiving rectal acetaminophen (median 10 h, inter-quartile range 9-11 h) compared with those receiving i.v. acetaminophen (7, 6-10 h) with a P-value of 0.01 by log-rank test for equality in survivor function. Few children in either group required rescue analgesia within the first 6 h with differences between the groups being most prominent in the period from 6 to 10 h. CONCLUSIONS: Rectal acetaminophen 40 mg kg(-1) provides longer analgesia for moderately painful procedures when compared with 15 mg kg(-1) acetaminophen i.v.

The G-308A variant of the Tumor Necrosis Factor-alpha (TNF-alpha) gene is not associated with obesity, insulin resistance and body fat distribution.

BACKGROUND: Tumor Necrosis Factor-alpha (TNF-alpha) has been implicated in the pathogenesis of insulin resistance and obesity. The increased expression of TNF-alpha in adipose tissue has been shown to induce insulin resistance, and a polymorphism at position -308 in the promoter region ofTNF-alpha has been shown to increase transcription of the gene in adipocytes. Aim of this study is to investigate the role of the G-308A TNFalpha variant in obesity and to study the possible influence of this mutation on body fat distribution and on measures of obesity (including Fat Free Mass, Fat Mass, basal metabolic rate), insulin resistance (measured as HOMAIR), and lipid abnormalities. The G-308A TNFalpha polymorphism has been studied in 115 patients with obesity (mean BMI 33.9 +/- 0.5) and in 79 normal lean subjects (mean BMI 24.3 +/- 0.3). METHODS: The G-308A variant, detected by PCR amplification and Nco-1 digestion, determines the loss of a restriction site resulting in a single band of 107 bp [the (A) allele]. RESULTS: The (A) allele frequencies of the G-308A TNFalpha polymorphism were 13.1% in the obese group and 14.6% in the lean subjects, with no significant difference between the two groups. Furthermore, no association was found with BMI classes, body fat distribution, HOMAIR, and metabolic abnormalities. CONCLUSIONS: Our study did not detect any significant association of the G-308A TNFalpha polymorphism with obesity or with its clinical and metabolic abnormalities in this population. Our data suggests that, in our population, the G-308A TNFalpha polymorphism is unlikely to play a major role in the pathogenesis of these conditions.

The G972R variant of the insulin receptor substrate-1 (IRS-1) gene, body fat distribution and insulin-resistance.

AIMS/HYPOTHESIS: Insulin resistance is recognised as the core factor in the pathogenesis of Type II (non-insulin-dependent) diabetes mellitus, hypertension and atherosclerosis. Several studies indicate the possible role of mutations of the insulin receptor substrate-1 (IRS-1) gene in the pathogenesis of insulin-resistance and suggest a possible interaction between the IRS-1 gene and obesity, either by an effect on the development of obesity or by causing or aggravating the obesity-associated insulin resistance. Therefore, the prevalence of the G972R mutation of the IRS-1 gene was compared in 157 non-diabetic obese subjects (BMI > 30 m/kg2) and in 157 lean subjects (BMI < 28 m/kg2). By investigating the relation between this IRS-1 mutation, measures of obesity and metabolic parameters, we explored the possible influence of this mutation on body fat distribution and insulin resistance. METHODS: The G972R mutation was detected by PCR amplification and BstN-1 restriction enzyme digestion. Data were analysed by univariate and multivariate analysis. RESULTS: The G972R allele was significantly more frequent in obese subjects than in lean subjects (p < 0.002); however, no difference was found between centrally and peripherally obese subjects. Obese G972R carriers had significantly higher BMI (p < 0.001), fasting insulin (p < 0.001), triglycerides (p < 0.03) and HOMAIR (p < 0.001) than obese non-carriers. No differences were observed between G972R carriers and non-carriers among control subjects. Multivariate analysis confirmed that the IRS-1 G972R mutation was significantly and independently associated with reduced insulin sensitivity (p < 0.009) in the obese group. CONCLUSION/INTERPRETATION: The G972R mutation of the IRS-1 gene associates with obesity, but not with fat distribution, in this Italian cohort, and within the obese subjects this IRS-1 variant strongly associates with metabolic parameters suggesting greater insulin-resistance. These findings indicate a possible interaction between the IRS-1 variant and obesity in worsening insulin sensitivity.

[Iatrogenic sequelae of pulmonary tuberculosis]. / Le sequelae iatrogene della tubercolosi polmonare.

OBJECTIVES: The purpose of this study is to underline how topical is the chapter of the sequelae of pulmonary tuberculosis and to try to make a classification. Pulmonary tuberculosis can be cured definitely or hesitate in disease (BK negative) that is totally independent from tuberculosis about their pathogenesis and clinical features. They are called sequelae. MATERIALS AND METHODS: We made a statistical analysis that investigate a group of 110 patients without active infection (BK negative) admitted in the hospital because of a sequela of pulmonary tuberculosis. Patients were treated in the past by collapse-therapy or by antibiotic-therapy until their spittle became negative for BK. RESULTS: A significant (p < 0.05) relationship between each kind of sequela, among the most important ones (fibrothorax, interstitial fibrosis, bronchiectasis, empyema with or without pleural fistula, parafibrotic emphysema), and type of treatment, results. CONCLUSIONS: The sequelae of tuberculosis of the lung are highly disadvantageous for people who are affected; are observed frequently; are closely dependent on what kind of treatment the patient has received; are classified in iatrogenic, not iatrogenic or mixed.

High frequency of polymorphism but no mutations found in the GLUT1 glucose transporter gene in NIDDM and familial obesity by SSCP analysis.

To evaluate whether a structural defect in the human glucose transporter gene GLUT1 could be involved in the aetiology of insulin resistance, a key factor of non-insulin-dependent diabetes mellitus (NIDDM) and obesity, we performed single-strand conformation polymorphism (SSCP) analysis in 40 subjects (20 NIDDM patients and 20 subjects with familial obesity). The GLUT1 gene, which is involved in basal glucose transport in most tissues, consists of ten exons and encodes a 492 amino acid protein. Population studies have shown a strong association between the X1 allele of an XbaI restriction fragment length polymorphism of the GLUT1 gene and NIDDM. We therefore performed SSCP analysis in NIDDM subjects known to carry at least one X1 allele. Variant SSCP patterns were detected in exons 2, 4, 5 and 9. Sequence analysis of the SSCP variants revealed the presence, in all exons examined, of silent mutations consisting of single-nucleotide substitutions with no amino acid changes. Both NIDDM and obese patients showed a high frequency of polymorphism in the sequence (50% and 35%, respectively). We conclude that the GLUT1 gene is unlikely to play a role in the aetiology of NIDDM and obesity. However, the strong association between the GLUT1 gene and NIDDM, together with the recent family studies showing linkage between chromosome 1p and NIDDM warrant further studies on this chromosomal region.